The difficulty, the authors argue, is that paediatric varicoceles are not a single entity. They vary enormously in severity, in the side affected, in the age at which they appear, and in the degree to which the affected testicle lags behind its partner in size. Most adolescents with a varicocele are entirely asymptomatic and will never experience fertility problems, which makes aggressive intervention for everyone hard to justify. At the same time, a minority of patients do sustain progressive testicular damage, and the available evidence has never been strong enough to identify them reliably in advance. The result has been wide practice variation, with some surgeons repairing nearly every varicocele they see and others reserving surgery for extreme cases.

Understanding why a varicocele can harm the testicle requires a look at the underlying anatomy and physiology. The internal spermatic veins, which drain blood from the testis back toward the major abdominal vessels, lack effective valves in many individuals. On the left side, the vein takes a longer, more vertical course and empties into the left renal vein at a right angle, creating a column of blood under higher hydrostatic pressure — a configuration that explains why roughly 90 percent of varicoceles occur on the left. When venous drainage stalls, blood pools and flows backwards, or retrogradely, into the pampiniform plexus. Animal studies dating back to the 1980s showed that this reversal of flow raises intratesticular temperature and disrupts the countercurrent heat-exchange system that normally keeps the testis a few degrees cooler than body core temperature, a condition essential for spermatogenesis.

The downstream cellular consequences form a cascade that the review maps out in detail. Venous congestion produces relative hypoxia within the testicular tissue, stabilising hypoxia-inducible factor-1 alpha, a transcription factor that in turn upregulates vascular endothelial growth factor and drives abnormal angiogenesis. At the same time, impaired clearance of reactive metabolites promotes oxidative stress, which damages sperm DNA and membranes, while excess nitric oxide produced within the testis further dilates the spermatic veins in a self-reinforcing loop and interferes with steroidogenesis in the Leydig cells, the factories of testosterone. The net effect is a gradual decline in sperm production, rising germ-cell apoptosis and, in some patients, measurable shrinkage of the affected testis relative to the normal side.

That shrinkage — testicular volume asymmetry — is the single most important clinical warning sign. The review highlights evidence that adolescents with a volume difference greater than 20 percent between the two testes are at substantially higher risk of progressive gonadal dysfunction, whereas asymmetry below 10 percent is generally reassuring. Measurement matters here: ultrasound has largely displaced the Prader orchidometer because it provides reproducible, norm-referenced volumes across childhood and puberty, allowing clinicians to track catch-up growth or deterioration over serial visits. Interestingly, some degree of asynchronous testicular growth during puberty is transient in many boys, and studies of non-operative management have documented spontaneous catch-up growth without surgery, reinforcing the case for careful surveillance in milder presentations.

Doppler ultrasonography adds a second, more technical dimension to risk assessment. Beyond confirming the dilated veins, duplex scanning can quantify peak retrograde flow velocity — the speed at which blood flows backwards through the spermatic vein during a Valsalva manoeuvre. The review identifies a peak retrograde flow above 38 centimetres per second as a threshold associated with persistent, progressive or new-onset testicular asymmetry, and later work has linked high retrograde flow to elevated sperm DNA fragmentation in young adults. A low-flow, low-grade varicocele with minimal asymmetry and normal hormonal markers sits firmly in the observation camp; a high-flow, high-grade lesion with measurable testicular loss pushes decisively toward intervention.

Laboratory markers complete the risk picture. Serum inhibin B, secreted by Sertoli cells, reflects the health of the seminiferous tubules, while follicle-stimulating hormone, luteinising hormone and testosterone track the hormonal axis that governs testicular function. In adolescents old enough to produce a semen sample, semen analysis remains the most direct readout of spermatogenesis, and abnormalities in multiple parameters — particularly a reduced total motile sperm count — combined with hormonal changes argue for repair. The authors acknowledge real-world barriers: many teenagers and parents are uncomfortable with semen collection, and attitudes surveys have documented reluctance on all sides. Nevertheless, they argue that in appropriate patients these tests transform an educated guess into a genuinely individualised decision.

When treatment is chosen, the modern options are safer and more refined than the operations of previous generations. Surgical approaches range from the retroperitoneal Palomo procedure, often performed laparoscopically, to microsurgical inguinal and subinguinal techniques that use an operating microscope to spare the testicular artery and lymphatic vessels. Artery and lymphatic preservation matters: large series have shown that accidental arterial ligation can cause testicular atrophy, and that lymphatic-sparing techniques dramatically reduce the most common complication, hydrocele formation. Percutaneous embolisation, in which an interventional radiologist occludes the incompetent vein with coils through a small catheter, offers a minimally invasive alternative with comparable technical success in selected patients. Across modalities, the review concludes that contemporary varicocele repair is safe, technically effective, and likely to confer a modest benefit on testicular volume and future fertility parameters.

Two clinical scenarios deserve special mention. First, pain: although most varicoceles are silent, a minority cause chronic scrotal discomfort, and the evidence summarised in the review indicates that repair is highly effective for appropriately selected patients, with longer duration of preoperative pain predicting better outcomes. Second, bilaterality: while the left side dominates clinically, venographic and fluid-mechanics studies suggest that varicocele is fundamentally a bilateral disease of the venous drainage system, and bilateral or isolated right-sided varicoceles — the latter occasionally signalling an anatomical obstruction that warrants abdominal imaging — carry a higher risk profile and warrant a lower threshold for both investigation and treatment.

The synthesis that emerges is a risk-stratified model rather than a one-size-fits-all rule. Low-grade varicoceles with less than 10 percent volume asymmetry, normal hormone and semen parameters, and low retrograde flow are candidates for observation with periodic reassessment through adolescence. High-grade or bilateral varicoceles, asymmetry exceeding 20 percent, peak retrograde flow above 38 centimetres per second, and multiple abnormalities on semen and hormone testing identify patients likely to benefit from early repair. Crucially, the authors emphasise shared decision-making: because most affected teenagers remain asymptomatic and the long-term fertility stakes are probabilistic rather than certain, patient and family preferences must sit alongside the objective findings. For a condition that has divided paediatric urologists for half a century, the message is neither watch everything nor fix everything, but measure carefully, stratify honestly and let the evidence — and the adolescent — guide the choice.

Subject of Research: Risk-stratified management of paediatric varicocele, weighing observation against surgical repair in adolescents

Article Title: Observation or treatment of paediatric varicoceles: revisiting the evidence

Article References: Buchinsky, D. S., Naelitz, B. D., Siva, J., Vallabhaneni, S., Momtazi-Mar, L., Klock, J., Hannick, J. H., Lundy, S. D., Weaver, J., & Woo, L. (2026). Observation or treatment of paediatric varicoceles: revisiting the evidence. Nature Reviews Urology. https://doi.org/10.1038/s41585-026-01187-y

Image Credits: AI Generated

DOI: 10.1038/s41585-026-01187-y

Keywords: paediatric varicocele, adolescent urology, testicular volume asymmetry, Doppler ultrasonography, peak retrograde flow, varicocelectomy, embolisation, male fertility, sperm DNA fragmentation, inhibin B, shared decision-making, Nature Reviews Urology